We tested whether the responsiveness of the kidney to basal renal sympathetic nerve activity (RSNA) or hypoxia-induced reflex increases in RSNA, is enhanced in angiotensin-dependent hypertension in rabbits. Mean arterial pressure, measured in conscious rabbits, was similarly increased (+16±3 mmHg) four weeks after clipping the left (n=6) or right (n=5) renal artery, or commencing a subcutaneous angiotensin II infusion (n=9), but was not increased after sham-surgery (n=10). Under pentobarbital anesthesia, reflex increases in RSNA (51±7%) and whole body norepinephrine spillover (90±17%), and the reductions in glomerular filtration rate (-27±5%), urine flow (-43±7%), sodium excretion (-40±7%), and renal cortical perfusion (-7±3%) produced by hypoxia were similar in normotensive and hypertensive groups. Hypoxia-induced increases in renal norepinephrine spillover tended to be less in hypertensive (1.1±0.5 ng/min) than normotensive (3.7±1.2 ng/min) rabbits but basal overflow of endogenous and exogenous dihydroxyphenolglycol was greater. Renal plasma renin activity (PRA) overflow increased less in hypertensive (22±29 ng/min) than normotensive rabbits (253±88 ng/min) during hypoxia. Acute renal denervation did not alter renal hemodynamics or excretory function, but reduced renal PRA overflow. Renal vascular and excretory responses to reflex increases in RSNA induced by hypoxia are relatively normal in angiotensin-dependent hypertension, possibly due to the combined effects of reduced neural norepinephrine release and increased postjunctional reactivity. In contrast, neurally-mediated renin release is attenuated. These findings do not support the hypothesis that enhanced neural control of renal function contributes to maintenance of hypertension associated with activation of the renin/angiotensin system.